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Breed‐specific pro‐inflammatory cytokine production as a predisposing factor for susceptibility to sepsis in the dog
Author(s) -
Nemzek Jean A.,
Agrodnia Marta D.,
Hauptman Joe G.
Publication year - 2007
Publication title -
journal of veterinary emergency and critical care
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.886
H-Index - 47
eISSN - 1476-4431
pISSN - 1479-3261
DOI - 10.1111/j.1476-4431.2006.00215.x
Subject(s) - breed , medicine , enteritis , cytokine , sepsis , purebred , veterinary medicine , immunology , gastroenterology , biology , zoology
Objective: To determine whether 2 dog breeds with a high risk for parvoviral enteritis, a disease associated with sepsis, produce stronger pro‐inflammatory cytokine responses to a stimulus than dogs with a lower risk. Design: Blinded comparison. Setting: University outpatient clinic. Animals: Healthy, unrelated, purebred Doberman Pinschers ( n =10) and Rottweilers ( n =9) with age‐matched mixed‐breed dogs ( n =7). Interventions: Heparinized, whole‐blood samples were collected from each dog and incubated for 6 hours with lipopolysaccharide. Plasma was collected, and bioassays were used to determine the concentrations of TNF‐α and IL‐6. The mean values obtained from the high‐risk breeds were compared with the mean obtained from the mixed‐breeds. Measurements and main results: The mean TNF‐α production from dogs with a high risk for parvoviral enteritis (1321±161 pg/mL; Doberman Pinscher and Rottweiler) was greater ( P <0.05) than that from lower risk, mixed‐breed dogs (674±186 pg/mL). There were no differences in TNF‐α levels between Doberman (1128±247 pg/mL) and Rottweiler (1563±pg/mL) breeds or between any breeds with regard to IL‐6 production. Conclusions: The magnitude of TNF‐α production by peripheral blood monocytes was the greatest in the dogs with breed‐related risk for parvoviral enteritis. However, additional studies are needed to prove a causal relationship between high TNF and predilection for parvoviral enteritis. Regardless, breed appears to be a predisposing factor for variations in cytokine production that could impact the host response to infection and other inflammatory insults.